Evaluation of human fibroblast growth factor 23 (FGF-23) C-terminal and intact enzyme-linked immunosorbent-assays in end-stage renal disease patients.

Hyperphosphataemia, calcitriol deficency and secondary hyperparathyroidism (sHPT) are common complications in end-stage chronic kidney diseases (CKD). Fibroblast Growth Factor 23 (FGF-23) is a phosphaturic peptide, secreted by the osteoblast precursors, that also inhibits renal 1-alpha-hydroxylase activitiy and tubular phosphate reabsorption by the inhibition of sodium-dependant renal phosphate transport (Na-Pi-IIa). Consequences are a decreaese of serum 1,25 dihydroxyvitamin D3 and phosphaturia. Therefore, FGF-23 plays a role in hyperphosphataemia in association with CKD and may be involved in the pathogenesis of sHPT. Increased FGF-23 may contribute to maintaining a normal serum phoshpate level in face of a processing CKD, but if the creatinine clearance is reduced to lower than 30 ml/min the capacity of this regulative mechanism ends and hyperphosphataemia results. In our investigation of end-stage renal diseases markedly increased serum FGF-23, associated with hyperphosphataemia, phosphaturia and decreased serum calcitriol and sHPT, were found. Furthermore preanalytical testing for the stability of FGF-23 was performed by comparing samples which were stored at -20 degrees C with samples that have been stored for 6 days at +4 degrees C. The simultaneous investigation of serum and EDTA plasma FGF-23 certifies the advantage of EDTA plasma in subjects with an intact renal function.